Chapter 13. Memory, Learning, and Development
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By Hanae Armitage Playing an instrument is good for your brain. Compared to nonmusicians, young children who strum a guitar or blow a trombone become better readers with better vocabularies. A new study shows that the benefits extend to teenagers as well. Neuroscientists compared two groups of high school students over 3 years: One began learning their first instrument in band class, whereas the other focused on physical fitness in Junior Reserve Officers’ Training Corps (JROTC). At the end of 3 years, those students who had played instruments were better at detecting speech sounds, like syllables and words that rhyme, than their JROTC peers, the team reports online today in the Proceedings of the National Academy of Sciences. Researchers know that as children grow up, their ability to soak up new information, especially language, starts to diminish. These findings suggest that musical training could keep that window open longer. But the benefits of music aren’t just for musicians; taking up piano could be the difference between an A and a B in Spanish class. © 2015 American Association for the Advancement of Science
Results from tests of the drug, announced this week, show that it breaks up plaques in mice affected with Alzheimer’s disease or Parkinson’s disease, and improves the memories and cognitive abilities of the animals. Other promising results in rats and monkeys mean that the drug developers, NeuroPhage Pharmaceuticals, are poised to apply for permission to start testing it in people, with trials starting perhaps as early as next year. The drug is the first that seems to target and destroy the multiple types of plaque implicated in human brain disease. Plaques are clumps of misfolded proteins that gradually accumulate into sticky, brain-clogging gunk that kills neurons and robs people of their memories and other mental faculties. Different kinds of misfolded proteins are implicated in different brain diseases, and some can be seen within the same condition (see “Proteins gone rogue”, below). One thing they share, however, is a structural kink known as a canonical amyloid fold, and it is this on which the new drug acts (Journal of Molecular Biology, DOI: 10.1016/j.jmb.2014.04.015). Animal tests show that the drug reduces levels of amyloid beta plaques and tau protein deposits implicated in Alzheimer’s disease, and the alpha-synuclein protein deposits thought to play a role in Parkinson’s disease. Tests on lab-made samples show that the drug also targets misfolded transthyretin, clumps of which can clog up the heart and kidney, and prion aggregates, the cause of CJD, another neurodegenerative condition. Because correctly folded proteins do not have the distinct “kink”, the drug has no effect on them. © Copyright Reed Business Information Ltd.
by Sarah Schwartz Brainlike cell bundles grown in a lab may expose some of the biological differences of autistic brains. Researchers chemically reprogrammed human stem cells into small bundles of functional brain cells that mimic the developing brain. These “organoids” appear to be different when built with cells from autistic patients compared with when they are built with cells from the patients’ non-autistic family members, researchers report July 16 in Cell. The brainlike structures created from cells taken from autistic children showed increased activity in genes that control brain-cell growth and development. Too much activity in one of these genes led to an overproduction of a certain type of brain cell that suppresses the activity of other brain cells. At an early stage of development, the miniature organs grown from autistic patients’ stem cells also showed faster cell division rates than those grown from the cells of non-autistic relatives. Though the study was small, using cells from only four autistic patients and eight family members, the results may indicate common factors underlying autism, the scientists say. © Society for Science & the Public 2000 - 2015.
Link ID: 21186 - Posted: 07.18.2015
by Sarah Zielinski It may not be polite to eavesdrop, but sometimes, listening in on others’ conversations can provide valuable information. And in this way, humans are like most other species in the animal world, where eavesdropping is a common way of gathering information about potential dangers. Because alarm calls can vary from species to species, scientists have assumed that eavesdropping on these calls of “danger!” requires some kind of learning. Evidence of that learning has been scant, though. The only study to look at this topic tested five golden-mantled ground squirrels and found that the animals may have learned to recognize previously unknown alarm calls. But the experiment couldn’t rule out other explanations for the squirrels’ behavior, such as that the animals had simply become more wary in general. So Robert Magrath and colleagues at Australian National University in Canberra turned to small Australian birds called superb fairy-wrens. In the wild, these birds will flee to safety when they hear unfamiliar sounds that sound like their own alarm calls, but not when they hear alarm calls that sound different from their own. There’s an exception, though: They’ll take to cover in response to the alarm calls of other species that are common where they live. That suggests the birds learn to recognize those calls. In the lab, the team played the alarm call from a thornbill or a synthetic alarm call for 10 fairy-wrens. The birds didn’t respond to the noise. Then the birds went through two days of training in which the alarm call was played as a mock predator glided overhead. Another group of birds heard the calls but there was no pretend predator. © Society for Science & the Public 2000 - 2015
By Claire Asher Even fish have role models. In a new study, researchers paired up inexperienced fathead minnows (Pimephales promelas, pictured) with two types of mentors: a minnow raised in an environment free of predators or a minnow raised in a dangerous one simulated by the odors of predatory pike and sturgeon. Fish from dangerous environments were fearful of the smell of both unknown and familiar predators, whereas fish that grew up in safety hid when they smelled a known predator but were curious about new smells. Both types of fish passed on their fears to their protégés: Minnows that spent time with fish raised in dangerous environments were scared of all smells they came across, but those that learned from fish raised in safety feared only specific predators and took new experiences in stride, the team reports online this week in the Proceedings of the Royal Society B. The authors say this is the first experiment to show that environment can influence the social transmission of fear and reveals how risk aversion can be learned. The researchers also suggest their study may shed light on how fear disorders such as post-traumatic stress disorder (PTSD) develop in humans, which research shows can be influenced by social environment; PTSD symptoms can be acquired from friends or family who have suffered trauma, for example. © 2015 American Association for the Advancement of Science
By Emily Underwood Glance at a runner's wrist or smartphone, and you'll likely find a GPS-enabled app or gadget ticking off miles and minutes as she tries to break her personal record. Long before FitBit or MapMyRun, however, the brain evolved its own system for tracking where we go. Now, scientists have discovered a key component of this ancient navigational system in rats: a group of neurons called "speed cells" that alter their firing rates with the pace at which the rodents run. The findings may help explain how the brain maintains a constantly updated map of our surroundings. In the 1970s, neuroscientist John O'Keefe, now at University College London, discovered neurons called place cells, which fire whenever a rat enters a specific location. Thirty-five years later, neuroscientists May-Britt and Edvard Moser, now at the Norwegian University of Science and Technology in Trondheim, Norway, discovered a separate group of neurons, called grid cells, which fire at regular intervals as rats traverse an open area, creating a hexagonal grid with coordinates similar to those in GPS. The Mosers and O'Keefe shared last year's Nobel Prize in Physiology and Medicine for their findings, which hint at how the brain constructs a mental map of an animal's environment. Still mysterious, however, is how grid and place cells obtain the information that every GPS system requires: the angle and speed of an object's movement relative to a known starting point, says Edvard Moser, co-author of the new study along with May-Britt Moser, his spouse and collaborator. If the brain does indeed contain a dynamic, internal map of the world, "there has to be a speed signal" that tells the network how far an animal has moved in a given period of time, he says. © 2015 American Association for the Advancement of Science.
Keyword: Learning & Memory
Link ID: 21178 - Posted: 07.16.2015
By Fredrick Kunkle A new study suggests that Alzheimer’s disease may affect the brain differently in black people compared with whites. The research, conducted by Lisa L. Barnes at the Rush University Medical Center, suggests that African Americans are less likely than Caucasians to have Alzheimer’s disease alone and more likely to have other pathologies associated with dementia. These include the presence of Lewy bodies, which are abnormal proteins found in the brain, and lesions arising from the hardening of tiny arteries in the brain, which is caused mainly by high blood pressure and other vascular conditions. The findings suggest that researchers should seek different strategies to prevent and treat Alzheimer’s disease in blacks. While many therapeutic strategies focus on removing or modifying beta amyloid – a key ingredient whose accumulation leads to the chain of event triggering the neurodegenerative disease – the study suggests that possible treatments should pursue additional targets, particularly for African Americans. But the study also points up the critical need to enroll more black people in clinical trials. Although Barnes said the research was the largest sample of its kind, she also acknowledged that the sample is still small. And that’s at least partially because blacks, for a variety of cultural and historical reasons, are less likely to participate in scientific research.
Link ID: 21176 - Posted: 07.16.2015
Nikki Stevenson Autism may represent the last great prejudice we, as a society, must overcome. History is riddled with examples of intolerance directed at the atypical. We can sometime fear that which diverges from the “norm”, and sometimes that fear leads us to frame those who are different as being in some way lesser beings than ourselves. Intolerances take generations to overcome. Racism is an obvious, ugly example. Other horrifying examples are easy to find: take, for instance the intolerance faced by the gay community. Countless gay people were diagnosed with “sociopathic personality disturbance” based upon their natural sexuality. Many were criminalised and forced into institutions, the “treatments” to which they were subject akin to torture. How many believed they were sociopathic and hated themselves, wishing to be free from the label they had been given? How many wished to be “cured” so that they could live their lives in peace? The greatest crime was the damage perpetuated by the image projected upon them by those claiming to be professionals. Autism is framed as a disability, with mainstream theories presenting autism via deficit models. Popular theory is often passed off as fact with no mention of the morphic nature of research and scientific process. Most mainstream theory is silent regarding autistic strengths and atypical ability; indeed, what is in print often presents a damning image of autism as an “epidemic”. Hurtful words such as risk, disease, disorder, impairment, deficit, pedantic, obsession are frequently utilised. © 2015 Guardian News and Media Limited
Link ID: 21175 - Posted: 07.16.2015
By Lauran Neergaard, New research suggests it may be possible to predict which preschoolers will struggle to read — and it has to do with how the brain deciphers speech when it's noisy. Scientists are looking for ways to tell, as young as possible, when children are at risk for later learning difficulties so they can get early interventions. There are some simple pre-reading assessments for preschoolers. But Northwestern University researchers went further and analyzed brain waves of children as young as three. How well youngsters' brains recognize specific sounds — consonants — amid background noise can help identify who is more likely to have trouble with reading development, the team reported Tuesday in the journal PLOS Biology. If the approach pans out, it may provide "a biological looking glass," said study senior author Nina Kraus, director of Northwestern's Auditory Neuroscience Laboratory. "If you know you have a three-year-old at risk, you can as soon as possible begin to enrich their life in sound so that you don't lose those crucial early developmental years." Connecting sound to meaning is a key foundation for reading. For example, preschoolers who can match sounds to letters earlier go on to read more easily. Auditory processing is part of that pre-reading development: If your brain is slower to distinguish a "D" from a "B" sound, for example, then recognizing words and piecing together sentences could be affected, too. What does noise have to do with it? It stresses the system, as the brain has to tune out competing sounds to selectively focus, in just fractions of milliseconds. And consonants are more vulnerable to noise than vowels, which tend to be louder and longer, Kraus explained. ©2015 CBC/Radio-Canada
OLIVER SACHGAU Marc Lewis spends a lot of his time thinking about addiction. He has good reason to: In his 20s he struggled with his own addiction to opiates. He was eventually able to quit, and began researching addiction and neuroscience. Mr. Lewis became a professor of developmental psychology at the University of Toronto in 1989, and moved to Radboud University in the Netherlands in 2010. His new book, The Biology of Desire: Why Addiction is Not a Disease, looks at the neuroscience of addiction, mixing personal narratives with scientific data. The book will be released in Canada on Aug. 4. You argue addiction is not a disease, but an example of very normal brain activity. What do you mean? [It’s] an exaggerated form of learning. Let’s put it that way. People in neuroscience agree that addiction corresponds with brain changes, and that’s the basis of the disease argument: That addiction changes the brain, or hijacks the brain, as they say. As though it were a pathology or disease process. Whereas I argue that all learning changes – the brain is designed to change – but when you have highly motivated learning, especially something that gets repeated over and over, then the learning curve rises extremely rapidly, and you have a kind of exaggerated learning phenomenon, where the learning is deep and specialized, and blots out other available habits or other available perceptions. You chose to mix hard scientific data with these anecdotal stories. How come? I love that way of writing. It seems to me so amazing that brain changes are going on at the same time as lived experiences: The moment-to-moment changes of thoughts and feelings are completely yoked to changes and activity in your brain, but it’s almost impossible to tell both stories at the same time, because one is under the skin, in terms of cell firings and electrochemical impulses and stuff, and the other one is in terms of behavior and human values and norms and so forth. © Copyright 2015 The Globe and Mail Inc
By Ferris Jabr Newborns are hardly blank slates devoid of knowledge and experience, contrary to historical notions about the infant mind. Sensory awareness and learning start in the womb, as the recently reinvigorated study of fetal perception has made clearer than ever. In the past few years lifelike images and videos created by 3-D and 4-D ultrasound have divulged much more about physiology and behavior than the blurry 2-D silhouettes of typical ultrasound. And noninvasive devices can now measure electrical activity in the developing brain of a fetus or newborn. Recent insights gleaned from such tools provide a rich portrait of how a fetus uses its budding brain and senses to learn about itself and the outside world well before birth. Such research has improved care for preterm babies, suggesting the benefits of dim lights, familiar and quiet voices, and lots of comforting skin contact between mother and child. © 2015 Scientific American
Keyword: Development of the Brain
Link ID: 21161 - Posted: 07.13.2015
Zoë Corbyn Jesper Noehr, 30, reels off the ingredients in the chemical cocktail he’s been taking every day before work for the past six months. It’s a mixture of exotic dietary supplements and research chemicals that he says gives him an edge in his job without ill effects: better memory, more clarity and focus and enhanced problem-solving abilities. “I can keep a lot of things on my mind at once,” says Noehr, who is chief technology officer for a San Francisco startup. The chemicals he takes, dubbed nootropics from the Greek “noos” for “mind”, are intended to safely improve cognitive functioning. They must not be harmful, have significant side-effects or be addictive. That means well-known “smart drugs” such as the prescription-only stimulants Adderall and Ritalin, popular with swotting university students, are out. What’s left under the nootropic umbrella is a dizzying array of over-the-counter supplements, prescription drugs and unclassified research chemicals, some of which are being trialled in older people with fading cognition. There is no official data on their usage, but nootropics as well as other smart drugs appear popular in the Silicon Valley. “I would say that most tech companies will have at least one person on something,” says Noehr. It is a hotbed of interest because it is a mentally competitive environment, says Jesse Lawler, a LA based software developer and nootropics enthusiast who produces the podcast Smart Drug Smarts. “They really see this as translating into dollars.” But Silicon Valley types also do care about safely enhancing their most prized asset – their brains – which can give nootropics an added appeal, he says. © 2015 Guardian News and Media Limited
Patricia Neighmond Some antidepressants may increase the risk of birth defects if taken early in pregnancy, while others don't seem to pose the same risks, a study finds. The question of whether antidepressants can cause birth defects has been debated for years, and studies have been all over the map. That makes it hard for women and their doctors to make decisions on managing depression during pregnancy. To try to untangle the question, researchers at the Centers for Disease Control and Prevention analyzed federal data on more than 38,000 women who gave birth between 1997 and 2009. They looked at the number of birth defects among babies and asked women whether they took any antidepressants in the month before getting pregnant or during the first three months of pregnancy. The study, published Wednesday in The BMJ, found no association between the most commonly used antidepressant, sertraline (Zoloft), and birth defects. Forty percent of the women who took antidepressants took sertraline. They also found no increased risk of birth defects with the antidepressants citalopram (Celexa) and escitalopram (Lexapro). But the analysis did find an association between birth defects and the antidepressants fluoxetine (Prozac) or paroxetine (Paxil). That included heart defects, abdominal wall defects, and missing brain and skull defects with paroxetine, and heart wall defects and irregular skull shape with fluoxetine. The relative risk increased 2 to 3.5 times, depending on the defect and the medication. That may sound like a lot, but Jennita Reefhuis, an epidemiologist and lead researcher in the study, says "the overall risk is still small." © 2015 NPR
By Sarah C. P. Williams The next time you forget where you left your car keys, you might be able blame an immune protein that builds up in your blood as you age. The protein impairs the formation of new brain cells and contributes to age-related memory loss—at least in mice, according to a new study. Blocking it could help prevent run-of-the-mill memory decline or treat cognitive disorders, the researchers say. “The findings are really exciting,” says neurologist Dena Dubal of the University of California, San Francisco (UCSF), who was not involved in the study. “The importance of this work cannot be underestimated as the world’s population is aging rapidly.” Multiple groups of scientists have shown that adding the blood of older mice to younger animals’ bodies makes them sluggish, weaker, and more forgetful. Likewise, young blood can restore the memory and energy of older mice. Neuroscientist Saul Villeda of UCSF homed in on one actor he thought might be responsible for some of that effect: β2 microglobulin (B2M), an immune protein normally involved in distinguishing one’s own cells from invading pathogens. B2M has also been found at increased levels in patients with Alzheimer’s disease and other cognitive disorders. Villeda and his colleagues first measured B2M levels in the blood of both people and mice of different ages; they found that those levels increased with age. When the researchers injected B2M into 3-month-old mice, the young animals suddenly had trouble remembering how to complete a water maze, making more than twice as many errors after they’d already been trained to navigate the maze. Moreover, their brains had fewer new neurons than other mice. Thirty days later, however, when the protein had been cleared from their bodies, the animals' memory troubles were gone as well, and the number of newly formed brain cells was back to normal. © 2015 American Association for the Advancement of Science
By Michael T. Ullman and Mariel Y. Pullman The human brain possesses an incredible capacity to adapt to new conditions. This plasticity enables us not only to constantly learn but also to overcome brain injury and loss of function. Take away one capability, and little by little we often compensate for these deficits. Our brain may be especially well suited to overcome limitations in the case of psychiatric or neurological conditions that originate early in life, what clinicians call neurodevelopmental disorders. Given the brain's considerable plasticity during early years, children with these disorders may have particular advantages in learning compensatory strategies. It now appears that a single brain system—declarative memory—can pick up slack for many kinds of problems across multiple neurodevelopmental disorders. This system, rooted in the brain's hippocampus, is what we typically refer to when we think of learning and memory. It allows us to memorize facts and names or recall a first grade teacher or a shopping list. Whereas other memory systems are more specialized—helping us learn movements or recall emotional events, for instance—declarative memory absorbs and retains a much broader range of knowledge. In fact, it may allow us to learn just about anything. Given declarative memory's powerful role in learning, one might expect it to help individuals acquire all kinds of compensatory strategies—as long as it remains functional. Indeed, research suggests that it not only remains largely intact but also compensates for diverse impairments in five common conditions that are rarely studied in conjunction: autism spectrum disorder, obsessive-compulsive disorder (OCD), Tourette's syndrome, dyslexia and developmental language disorder (which is often referred to as specific language impairment, or SLI). © 2015 Scientific American
Keyword: Learning & Memory
Link ID: 21143 - Posted: 07.07.2015
By David Robson William’s internal clock is eternally jammed at 13:40 on 14 March 2005 – right in the middle of a dentist appointment. A member of the British Armed Forces, he had returned to his post in Germany the night before after attending his grandfather’s funeral. He had gym in the morning, where he played volleyball for 45 minutes. He then entered his office to clear a backlog of emails, before heading to the dentist’s for root-canal surgery. “I remember getting into the chair and the dentist inserting the local anaesthetic,” he tells me. After that? A complete blank. It is as if all new memories are being written in invisible ink that slowly disappears. Since then, he has been unable to remember almost anything for longer than 90 minutes. So while he can still tell me about the first time he met the Duke of York for a briefing at the Ministry of Defence, he can’t even remember where he’s living now; he wakes up every morning believing he is still in Germany in 2005, waiting to visit the dentist. Without a record of new experiences, the passing of time means nothing to him. Today, he only knows that there is a problem because he and his wife have written detailed notes on his smartphone, in a file labelled “First thing – read this”. It is as if all new memories are being written in invisible ink that slowly disappears. How could minor dental work have affected his brain in such a profound way? This real-life medical mystery offers a rare glimpse at the hidden depths of the brain’s workings. © 2015 BBC.
Keyword: Learning & Memory
Link ID: 21137 - Posted: 07.06.2015
By Adrian Cho Whether they're from humans, whales, or elephants, the brains of many mammals are covered with elaborate folds. Now, a new study shows that the degree of this folding follows a simple mathematical relationship—called a scaling law—that also explains the crumpling of paper. That observation suggests that the myriad forms of mammalian brains arise not from subtle developmental processes that vary from species to species, but rather from the same simple physical process. In biology, it rare to find a mathematical relationship that so tightly fits all the data, say Georg Striedter, a neuroscientist at the University of California, Irvine. "They've captured something," he says. Still, Striedter argues that the scaling law describes a pattern among fully developed brains and doesn't explain how the folding in a developing brain happens. The folding in the mammalian brain serves to increase the total area of the cortex, the outer layer of gray matter where the neurons reside. Not all mammals have folded cortices. For example, mice and rats have smooth-surfaced brains and are "lissencephalic." In contrast, primates, whales, dogs, and cats have folded brains and are "gyrencephalic." For decades, scientists have struggled to relate the amount of folding in a species' brain to some other characteristic. For example, although animals with tiny brains tend to have smooth ones, there is no clean relationship between the amount of folding—measured by the ratio of the total area of the cortex to the exposed outer surface of the brain—and brain mass. Make a plot of folding versus brain mass for various species and the data points fall all over and not on a unified curve. Similarly, there is no clean relationship between the amount of folding and the number of neurons, the total area of the cortex, or the thickness of the cortex. © 2015 American Association for the Advancement of Science
By SINDYA N. BHANOO It may be possible to diagnose autism by giving children a sniff test, a new study suggests. Most people instinctively take a big whiff when they encounter a pleasant smell and limit their breathing when they encounter a foul smell. Children with autism spectrum disorder don’t make this natural adjustment, said Liron Rozenkrantz, a neuroscientist at the Weizmann Institute of Science in Israel and one of the researchers involved with the study. She and her colleagues report their findings in the journal Current Biology. They presented 18 children who had an autism diagnosis and 18 typically developing children with pleasant and unpleasant odors and measured their sniff responses. The pleasant smells were rose and soap, and the unpleasant smells were sour milk and rotten fish. Typically developing children adjusted their sniffing almost immediately — within about 305 milliseconds. Children with autism did not respond as rapidly. As they were exposed to the smells, the children were watching a cartoon or playing a video game. “It’s a semi-automated response,” Ms. Rozenkrantz said. “It does not require the subject’s attention.” Using the sniff test alone, the researchers, who had not been told which children had autism, were able to correctly identify those with autism 81 percent of the time. They also found that the farther removed an autistic child’s sniff response was from the average for typically developing children, the more severe the child’s social impairments were. © 2015 The New York Times Company
By SINDYA N. BHANOO Learning can be traced back to individual neurons in the brain, according to a new study. “What we wanted to do was see if we could actually create a new association — a memory — and see if we would be able to see actual change in the neurons,” said Matias Ison, a neuroscientist at the University of Leicester in England and one of the study’s authors. He and his colleagues were able to monitor the brain activity of neurosurgical patients at UCLA Medical Center. The patients already had electrodes implanted in their medial temporal lobes for clinical reasons. The patients were first presented with images of notable people — like Jennifer Aniston, Clint Eastwood and Halle Berry. Then, they were shown images of the same people against different backdrops — like the Eiffel Tower, the Leaning Tower of Pisa and the Sydney Opera House. The same neurons that fired for the images of each of the actors also fired when patients were shown the associated landmark images. In other words, the researchers were able to watch as the patients’ neurons recorded a new memory — not just of a particular person, but of the person at a particular place. © 2015 The New York Times Company
Keyword: Learning & Memory
Link ID: 21126 - Posted: 07.02.2015
Jon Hamilton If you run into an old friend at the train station, your brain will probably form a memory of the experience. And that memory will forever link the person you saw with the place where you saw them. For the first time, researchers have been able to see that sort of link being created in people's brains, according to a study published Wednesday in the journal Neuron. The process involves neurons in one area of the brain that change their behavior as soon as someone associates a particular person with a specific place. "This type of study helps us understand the neural code that serves memory," says Itzhak Fried, an author of the paper and head of the Cognitive Neurophysiology Laboratory at UCLA. It also could help explain how diseases like Alzheimer's make it harder for people to form new memories, Fried says. The research is an extension of work that began more than a decade ago. That's when scientists discovered special neurons in the medial temporal lobe that respond only to a specific place, or a particular person, like the actress Jennifer Aniston. The experiment used a fake photo of actor Clint Eastwood and Pisa's leaning tower to test how the brain links person and place. More recently, researchers realized that some of these special neurons would respond to two people, but only if the people were connected somehow. For example, "a neuron that was responding to Jennifer Aniston was also responding to pictures of Lisa Kudrow," [another actress on the TV series Friends], says Matias Ison of the University of Leicester in the U.K. © 2015 NPR